OBJECTIVE: To present a case of shoulder impingement syndrome managed with a conservative multimodal treatment approach.

CLINICAL FEATURES: A patient had anterior shoulder pain and a diffuse ache in the right upper arm, with tenderness in the shoulder region on palpation. Shoulder range of motion was limited with pain and catching, coupled with limited and painful cervical motion. After physical and orthopedic examination, a clinical diagnosis of shoulder impingement syndrome was made.

INTERVENTIONS AND OUTCOMES: The patient underwent a multimodal treatment protocol including soft tissue therapy, phonophoresis, diversified manipulation; and rotator cuff and shoulder girdle muscle exercises. Outcomes included pain measurement; range of motion of the shoulder, and return to normal daily, work, and sporting activities. At the end of the treatment protocol the patient was symptom free with all outcome measures normal. The patient was followed up at 4 and 12 weeks and continued to be symptom free with full range of motion and complete return to normal daily and pre-treatment activities.

Practitioners of manual therapy commonly encounter patients presenting with shoulder pain and problems associated with the rotator cuff. In clinical frequency, shoulder pain is exceeded only by low-back and neck pain, [1] with about half the population having 1 episode of shoulder pain yearly. [2] Because of the complex nature of the shoulder, and its functional and anatomic relationship to spinal regions, shoulder pain has the potential to originate from a number of sources located within and distant to the shoulder. Therefore, a thorough understanding of the anatomy, biomechanics, and functional relationship of the shoulder and nearby spinal structures is prudent for successful rehabilitation outcomes.

Once a tissue in lesion diagnosis has been determined, treatment may be rendered accordingly. Some authors suggest that surgery is indicated for patients without rotator cuff tears after symptoms have been present for at least 1 year and have been nonresponsive to conservative care. [3] For most complaints, the treatment of choice is conservative. More serious pathology, such as neoplasm, [4] fracture, [5] tendon rupture, [6] and certain full thickness tears of the rotator cuff tendons, [7] must be ruled out.

The incidence of shoulder pain in a community setting is high, [1, 8, 9] with most data derived from medical literature. [1, 8, 9] Koes [8] investigated the prevalence of shoulder complaints in Dutch general practice and determined subacromial syndrome as the disorder most frequently diagnosed. In a community survey conducted by Chard [6] in a sample of 644 people, 170 (26%) reported shoulder pain with at least 70% involving the rotator cuff, including rotator cuff tendinitis and/or impingement or tears of the rotator cuff tendon. To date, there are no data investigating the prevalence of shoulder pain in a chiropractic setting.

The most common source of shoulder pain originates from the rotator cuff, with the most prevalent clinical diagnosis being impingement syndrome. [8–13]. Shoulder pain is a prevalent complaint in many athletes. The frequency of shoulder pain has been noted particularly in swimming, with estimates of 42% to 67% of competitive swimmers reporting shoulder pain during the course of their careers. [14]

Pink [15] reported shoulder pain in 66% of swimmers, 57% of professional pitchers, 44% of collegiate volleyball players, and 29% of collegiate javelin throwers. Morrison et al [10] reported in 2000 that 75% of patient presentations with rotator cuff tendinitis had an underlying impingement of the anterior acromion on the supraspinatus tendon and, occasionally, the infraspinatus.

Susceptible individuals to impingement and rotator cuff tendinitis also include those workers who use the arm repetitively in the horizontal position or above. [16] Various occupations, such as mill workers, carpenters, slaughterhouse workers, jackhammer operators, and shipyard welders, have all been noted to have elevated levels of shoulder pain relative to sedentary controls. [16–18]. The incidence of shoulder pain among workers has been linked to depressive symptoms, level of job control, and biomechanical risk factors. [19] The most important risk factors were repetitive use of a tool and working with the arms above shoulder level. [19] Shoulder pain and problems associated with the rotator cuff have a high prevalence in the general, sporting, and working community.

This article will discuss a common cause of shoulder pain and its conservative management in a chiropractic setting.

Discussion

To understand impingement syndrome a thorough understanding of shoulder anatomy is imperative. The shoulder girdle consists of 7 biomechanically related joints, which include the glenohumeral, suprahumeral, acromioclavicular, scapulocostal, sternoclavicular, sternocostal, and costovertebral joints. [1]
With respect to impingement syndrome, particular emphasis should be given to the suprahumeral joint. Classically, this area does not represent an articulation between 2 bones but has a strong functional anatomic relationship between associated structures that can be vulnerable to pathologic change (Fig 1).
Fig 1. The subacromial space (triangles) A, acromion; GT, greater tuberosity; CAL, coracoacromial ligament; B, biceps, long head; C, coracoid process.
The suprahumeral joint is also known as the suprahumeral space, subacromial space, or supraspinatus outlet. This region consists of the superior aspect of the humerus, inferior surface of the acromion, acromioclavicular joint, and the roof of the glenohumeral joint, namely the coracoacromial ligament. [1, 20-22] The subacromial space contains the tendons of the rotator cuff (supraspinatus, infraspinatus, and teres minor), the long head of the biceps, and the subdeltoid/acromial bursa. The height of this space in healthy shoulders is between 9 and 10 mm, whereby with radiographic measurements of less than 6 mm, is pathologic for compression of the rotator cuff. [22] The actual thickness of the rotator cuff tendon in this area is 5 to 6 mm, leaving very little clearance in cases of enlargement of the bursa or tendon or irregularities of the gliding surface. [9]

By definition, impingement syndrome refers to a pathologic condition in which there is irritation of the supraspinatus tendon secondary to abrasion against the under surface of the anterior one third of the acromion. [10] Neer [3] discusses the importance of the undersurface of the tendon and the potential changes that may occur due to repetitive friction and irritation in his landmark 3-stage impingement process classification.

Frieman [23] describes the impingement process as any anatomic or physiologic variant associated with a decrease in the space between the humeral head tuberosities, the rotator cuff, and the coracoacromial arch, because all can contribute to rotator cuff, impingement. This can lead to edema, inflammation, and bursitis, which can progress to degeneration and eventually to rotator cuff tearing. A commonly used definition describes the impingement syndrome as encroachment of the coracoacromial arch on the underlying mechanism of the rotator cuff (most commonly the supraspinatus tendon), a definition inherent in the diagnostic reasoning used in the case report. [24]

According to Fu, [25] impingement syndrome can be classified as either primary or secondary. Primary impingement syndrome results from pathologic narrowing of the subacromial space with impingement or irritation of the supraspinatus tendon secondary to abrasion against the under surface of the anterior one third of the acromion. Primary impingement involves a spectrum of lesions of tissues in the subacromial space; hence, a working knowledge of structural interrelationships will enhance understanding and, therefore, management of this process. Several factors have been implicated in this process.
Secondary impingement syndrome normally occurs in the younger individual and in athletes and is defined as a relative decrease in the supraspinatus outlet caused by instability of the glenohumeral joint. The symptoms can be attributed to rotator cuff tendinitis. [26] On examination, a positive impingement sign is evident. Often patients have symptoms of pain and weakness, especially with overhead activities. The symptoms of secondary impingement are often a result of rotator cuff overuse as a consequence of multidirectional glenohumeral instability. Scapulothoracic muscle weakness has also been attributed as a secondary cause of impingement syndrome due to a lack of scapula stability, causing a resultant glenohumeral instability. [26]

In the overhead or throwing athlete with repetitive and high-energy forces going through the shoulder, chronic stresses are placed on the stabilizing structures of the shoulder. With continued stress, the static stabilizers of the shoulder become hyperelastic, enabling anterior glenohumeral subluxation, contact with the coracoacromial arch, and ultimately leading to secondary subacromial impingement. This form of athletic injury is known as anterior glenohumeral instability of the shoulder and, as such, can be a secondary cause of impingement. The diagnosis of instability is made by a careful history and physical examination. Testing the shoulder for glenohumeral instability involves the use of the apprehension test followed by the relocation test. [27] The apprehension test is easily performed with the patient supine. The shoulder is placed in 90° of abduction and maximal external rotation, a gentle anteriorly directed force is applied by the practitioner with gentle fingertip pressure to the posterior humeral head. A positive test is apprehension and pain. [27-28]

Pain without apprehension may be indicative of primary impingement or mild anterior instability with secondary impingement. To differentiate primary instability from impingement the relocation test is used. This test is also performed in the same supine and arm position as the apprehension test; however, a posteriorly directed force is applied to the proximal humeral head, enabling further external rotation and reduction of any humeral head slippage. In patients with primary impingement no change in pain is noted; however, with primary instability and secondary impingement, a reduction of pain is experienced as the humeral head is reduced posteriorly, relieving the rotator cuff impingement on the posterosuperior glenoid rim. Factors contributing to the impingement process can be subdivided into intrinsic and extrinsic. [10, 22, 25-26]

The extrinsic causes are forces acting from outside the rotator cuff and are mechanical in origin and can be related to the anatomy of the coracoacromial arch. These causes are sometimes referred to as external anatomic impingement.10 Extrinsic causes may include muscle imbalances, functional changes associated with the rotator cuff and parascapular muscle groups, postural changes, and precipitating factors that can include training errors in athletes or occupational influences. [20, 22, 29] Extrinsic factors can contribute to either the primary or the secondary impingement process, with the key differentiating factor being the presence of glenohumeral instability in secondary impingement. Conservative therapy will focus on strengthening the rotator cuff to prevent instability.

Movement of the scapula and humerus are controlled by 2 muscle force couples that include the rotator cuff and scapula force couples. Any breakdown in their force couples will lead to uncoordinated muscular action and compressive pathology of the rotator cuff. [28]

Normal function of the shoulder is closely linked to the spine and posture, [29] and these regions including the shoulder should also undergo review in the determination of the cause of the shoulder pain. Slumping posture causes increased stress on posterior shoulder muscles, leading to muscular pain syndromes. [30] This may lead to increased incidence of interscapular pain as a consequence of excessive stretch placed on the levator scapulae muscle and some on the upper trapezius. Stress is also placed on the shoulder capsule and inhibition of the cuff muscles may occur, which can result in loss of the force couple of the shoulder at the glenohumeral joint.31 Shortening of the pectoral fascia, development of myofascial trigger points, and fibrosis may also occur. [31]

Altered scapulothoracic rhythm, including upper thoracic immobility, may combine to stress the levator scapulae and upper trapezius, creating myofascial trigger points and eventual adhesions. [20] Increased cervical lordosis and forward carriage of the shoulders may thus predispose shoulder muscle dysfunction. [29] This postural change leads to protraction of the scapulae with downward rotation and internal rotation of the humerus, hence the normal orientation of the plane of the scapula is changed. The resultant effect of this change are muscle imbalances around the shoulder and abnormal movement patterns during elevation of the glenohumeral joint.

These parascapular imbalances will lead to altered scapula position with scapula dysrhythmia. Associated weakness of the posterior cuff muscles may lead to loss of force couple at the glenohumeral joint and the inability of the cuff muscles to counter the upward shear of the humerus during elevation, leading to repetitive subacromial impingement of the humeral head. Low cervical joint immobility/dysfunction (C-5, C-6) has been implicated as a cause of spasm (muscular hypertonicity with resultant tightening or shortening of muscle fibers) of the rotator cuff muscles potentially disturbing the scapulo-humeral function, eventually leading to rotator cuff impingement. [32]

Precipitating factors [22] involve repetitive overuse in the overhead position (greater than 90° abduction). A good example of this can be the clerical worker who decides 1 weekend to sand and paint all the ceilings at home or the sportsperson who decides to swim 20 laps of the local pool for the first time in the summer season after having the winter off.

The intrinsic causes can be related to anatomic variants, degeneration, and vascularity of the rotator cuff. Table 1 lists anatomic variants that can be associated with rotator cuff impingement and have been cited in the literature. [23] The morphology of the acromion is an important factor that correlates with the predisposition toward rotator cuff impingement. The shapes of the acromion are classified into type I (flat), type II (curved), and type III (hooked). [31, 35]

Imaging the supraspinatus outlet clearly images the acromion and is often useful in cases of rotator cuff pathology. Useful imaging includes radiographs, advanced imaging such as computed tomography or magnetic resonance imaging (MRI), which is generally not necessary for impingement unless other pathology is suspected. When considering radiographic analysis a minimum of 4 views are necessary. According to Ciullo et al [33] these include 1) a 15° angle down, 15° internal rotation view for detail of the under surface of the acromion and the anterior inferior glenoid rim; 2) a 15° angle-up anterior-posterior film for acromioclavicular joint detail; 3) a supine axillary external rotation view for glenohumeral relationship; and 4) a 20° angled down scapular Y lateral view for the slope of the acromial arch.

The type III acromion has been found to contribute to 60% of rotator cuff problems.23 Recent evidence suggests a 58% correlation between rotator cuff tears and a type III acromion. [34] Besides acromial morphology, age, and sex have an independent association with rotator cuff pathology. [34-35] This morphology causes repetitive injury to the tendon and subsequent secondary changes within it. [31] Other mechanical factors listed in Table 2 can also contribute the impingement process. [10, 23]

Intrinsic causes can be also attributed to inflammatory changes within the cuff tendon. These intrinsic factors are related to the microvascular pattern of the rotator cuff tendon and to the zone of relative ischemia that occurs in specific arm positions as described by Rathburn and McNab. [36] This area of relative ischemia is the zone where most pathologic change (lesions) of the rotator cuff occurs and is known as the critical zone. Its location is approximately 1 cm from the insertion of the supraspinatus tendon on the greater tubercle of the humerus. [37] According to Rathbun and Macnab, [36] this region of avascularity was not seen in other cuff tendons other than the supraspinatus and the superior portion of the insertion of the infraspinatus. The biceps tendon also contains a small avascular area because it courses over the head of the humerus. The critical zone varies from being ischemic, when the vascular anastomosis of the tendon is constricted, to hyperemic when free blood flow is enabled.

This critical region has therefore been shown to be the area associated with tearing of the supraspinatus tendon. The tears usually occur longitudinally in the anterior portion of the cuff, and are often preceded by degenerative changes secondary to traction and compressive loading. [1]

The primary etiologic factor causing intrinsic changes has been reported to be multiple tension overload of the rotator cuff, especially the supraspinatus. [25] This may be caused by the morphology of the supraspinatus muscle, which has a much larger maximum belly size in comparison to its relatively smaller tendon size. [38] Subsequent fatigue, injury, and weakness of the cuff results in instability and muscle imbalances that produce upward humeral migration and subsequent soft tissue impingement. [26]

A less common type of impingement that can be added to the differential diagnosis is primary subcoracoid impingement. [22] This type of impingement occurs in the coracohumeral compartment, which is a space located between the tuberosity and lesser tubercle of the humerus. [22] This space contains the subcoracoid bursa, subscapularis bursa, and tendon.

Jobe [5] reports a type of impingement termed superior glenoid impingement. This condition has been reported in baseball players and in athletes of other overhead throwing sports. The condition is described as a chronic overuse condition in which contact is made between the superior glenoid labrum and internal fibers of the rotator cuff and the greater tuberosity.

Struhl [39] in a recent publication introduces the concept of anterior internal impingement in patients with signs and symptoms of classic impingement syndrome and arthroscopic evidence of articular side partial rotator cuff tear. With anterior internal impingement the source of pain arises from contact between the fragmented under surface of the rotator cuff and the anterior superior labrum.

Table 3 provides a list of differential diagnoses of impingement. Neer [3] clarified the concept of impingement in his landmark study, and divided the impingement process into 3 stages. The first stage was characterized by acute bursitis with subacromial edema and hemorrhage. This stage is usually observed in patients who are 30 years old or younger. The patient often presents with pain in the anterior or lateral aspect of the shoulder, which normally in the acute stages can be felt in military badge area of the shoulder (region of C5 dermatome). The pain can be a deep and dull ache with a catching sensation on upper limb elevation. Active and passive range of motion can be full, a painful arc is noted and a positive impingement sign is noted. The treatment is conservative with an expectation of full recovery. [3, 22]

Stage 2 is characterized by inflammation of the rotator cuff, fibrosis of the glenohumeral joint capsule and subacromial bursa with the possibility of progression to partial tears of the supraspinatus. The patient is often in the 20 to 40 year age groups with symptoms similar to that of stage 1. However, because of the fibrosis, there is normally a loss of passive and active range of motion in abduction and external rotation. Treatment still should be conservative.

Further continuation of the process results in the wear of the anterior aspect of the acromion on the greater tuberosity and the supraspinatus tendon, which eventually results in a full-thickness tear of the rotator cuff.

Stage 3 is most difficult to treat conservatively, with the patient normally being over 40 years of age. Muscle testing shows weakness of the external rotators and with tendon disruption, a positive drop arm, or empty can test. [3, 22]

Diagnosis of impingement syndrome and rotator cuff tendonitis is based on evaluation of presenting symptoms and physical examination. Supportive findings from radiographs maybe useful, whereby ultrasound or magnetic resonance imaging examination is not really necessary, unless pathology is suspected.

Initial patient assessment includes a thorough history, including pain, its location, referral or radiation, neurologic changes including associated weakness, numbness, paraesthesia or other symptoms and its effect on daily activities (including work), recreation, and sports. Shoulder function maybe measured by using paper-based scoring systems such as the subjective shoulder rating system, [40] Constant Murley, [41] or the UCLA scoring system. [42] Such questionnaires have been determined to be useful in determining function and disability as a consequence of shoulder pain, with good specificity, reliability, and reproducibility. [40-42]

The physical examination must be complete and performed carefully. Initially, the examination involves postural evaluation, inspection of the shoulder for muscle atrophy, swelling, skin color, elbow-carrying angle, scapular winging, acromioclavicular joint prominence, and continuity of the biceps tendon.

Active range of motion should be measured in abduction, internal/external rotation, flexion, extension, and adduction (multiple planes) with careful attention given to the presence of pain or symptoms. Limited active motion should be examined passively to help determine whether the restriction is caused by pain, weakness, stiffness, or muscle spasm. [43] With rotator cuff impingement syndromes, abduction shows a painful impingement arc approximately between 60° and 130°, going up or coming down. Most patients exhibit an increase in pain the higher the arm is elevated [9] Pain may also be noted in external or internal rotation, or adduction in the anterior aspect of the shoulder at the cuff insertion or lateral (C5) region of the upper arm.

Diagnosis of impingement is usually solidified by specific orthopedic testing. Two useful impingement tests are the Hawkin's and Neer's tests, although other variations exist., [43] The Hawkin's test is performed with the patients elbow flexed at 90° with the shoulder flexed forward to 90°. The practitioner maximally internally rotates the arm while stabilizing the scapula at the same time. The test reproduces the impingement sensation by causing the coracoacromial ligament to impinge on the supraspinatus tendon and greater tuberosity of the humerus. [29] The Neer impingement test is performed with the practitioner standing behind the shoulder while stabilizing the scapula. The patient elevates the arm into full flexion with slight internal rotation and forearm pronation. The test is considered positive if pain is reproduced in the last 10° to 15° of full glenohumeral flexion. [30]

With a positive Neer's or Hawkin's test, the most likely source of impingement is the rotator cuff tendon, generally the supraspinatus tendon. The sensitivity of Neer's test is 89% with a specificity of 31%, whereas the Hawkin's test has a sensitivity of 92% and specificity of 25%. [44] McDonald et al [45] reports 75% sensitivity for the Neer's test, compared with 92% for the Hawkin's sign. The authors conclude that both tests are sensitive for subacromial impingement but lack specificity when compared with arthroscopic findings. In a recent study by Roberts et al [46] with MRI analysis of the subacromial space in the impingement sign position, the rotator cuff insertion appeared to be in closest proximity to the anteroinferior acromion during the Hawkin's position. Hence, the authors suggest with a clinically positive Hawkin's sign, to be consistent with shoulder impingement. The biceps tendon must also be considered, as well as the subacromial bursa as a source of impingement. Radiographic studies will rule out any other potential source that may compromise the subacromial space including enlargement of the outer end of the clavicle/acromioclavicular joint, osteoarthritis, enlargement of the anterior inferior surface of the acromion, and osteophyte off the acromioclavicular joint and hypertrophy of the inferior acromioclavicular joint capsule. [47]

Instability should be examined as a potential cause of cuff pathology by passively stressing the shoulder to detect baseline laxity or multidirectional instability, which can contribute greatly to the impingement process. [9] Any excessive mobility of the glenohumeral joint may require additional activity of the cuff musculature to stabilize the joint.

Resisted muscle examination via manual testing is useful to determine any weakness or pain of the shoulder. Testing includes muscles of the scapula, biceps, and particularly the cuff muscles (supraspinatus, infraspinatus, subscapularis, and teres minor). Pain can mask the true evaluation of strength. Cuff muscle weakness is often seen in stage 2 or stage 3 of the impingement process. [9]

In the evaluation of the muscles of the scapula, the lateral scapula slide test can be used, which evaluates the ability of the posterior shoulder muscles to achieve scapula stabilization and positioning. [10] Measurements with a tape measure are taken in 3 positions: neutral with the arms at the side of the body and elbows flexed at 90°, 45° of shoulder elevation, and 90° of shoulder elevation. A measurement is taken from the inferior angle of the scapula and the T7 spinous process. A difference of 1 cm or more between the right and left sides in 2 of the 3 positions can be correlated with impingement. Scapula muscles can also be evaluated by manual muscle tests.

Palpation provides useful information that can greatly assist in making the diagnosis. Tenderness can be palpated in many of the shoulder girdle muscles, the acromioclavicular joint, the coracoid or coracoacromial ligaments, the rotator cuff insertions on the greater tuberosity of the humerus, and the biceps tendon. The inflamed biceps tendon may be an associated part of the impingement process and should be tested with the Speed's and Yergason's test. [28] Speed's test, according to Calis et al, [45] has a 69% sensitivity and a 56% specificity, and the Yergason test has a 37% and 86% sensitivity/specificity.

Finally, joint play and joint motion evaluation is imperative. This involves passive motion testing of periarticular tissue in which a specific joint is brought passively to its end range of motion. This area is known as the elastic barrier of resistance. This passive motion measures the joint range of motion and muscle flexibility and is used to measure joint play. This should include evaluation of the glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic articulations.

The patient presented in this article was treated with a treatment protocol that included a combination of therapies. The literature [15,21, 37, 45, 48-51] suggests that the multimodal approach is the appropriate direction via which shoulder problems can be successfully managed by using conservative measures.

The goal of this article is to highlight the multifactorial management often required to address the painful shoulder, not to determine or to show which treatment approach or particular therapy was more effective but to document a management protocol with an evidence-based foundation that would enable the clinician to achieve the goals of therapy in an effective and efficient way. A multimodal management protocol is important in treating the shoulder because of not only its complex anatomic structure and mechanical function but also its close relationship with structures adjacent to the shoulder, including the cervical and thoracic spines. However, because of the nature of a case presentation, it is limited by not having a control to allow for the passage of time.

In treating a painful shoulder, all biomechanically linked areas must be assessed as part of the treatment to determine whether one or all are the primary cause of the cuff problem. A good example of this is a slumping posture in a competitive swimmer. The rounded shoulders and increased thoracic kyphosis associated with this posture places increased demands on the rotator cuff and contributes to the impingement process. This postural change alters the mechanical function and orientation of the scapula and humerus, leading to muscular imbalances and abnormal movement patterns during glenohumeral elevation with associated weakness of the posterior cuff muscles. Therefore, this leads to a loss of force couple at the glenohumeral joint with resultant repetitive humeral head impingement. [20, 29, 52]

The outcome measures for the study were subjective improvement of pain, return to pretreatment activities, and restoration of full active and passive movements. The outcome measures were mainly subjective in nature and dependent on the response of the patient and the ability of the practitioner in conducting the orthopedic reassessment; therefore, allowing an element of examination bias. This particular area may be improved by using sensitive scoring systems. A good example of a scoring system includes the subjective shoulder rating system, UCLA scoring system or the highly sensitive Constant/Morley functional assessment of the shoulder. The benefit of using such a system lies in their reproducibility among different practitioners. [40-42] A more objective outcome measure can be achieved by the use of a goniometer. This case report presents an approach that combines aspects of traditional forms of chiropractic, physiotherapy, and medicine in the conservative treatment of patients presenting with these symptoms.

The individual therapies that were used in this treatment protocol have been derived from the literature (incorporating soft tissue therapy, manipulation, ultrasound, and exercises) and have been shown to be useful in the management of shoulder pain both singularly and in combination. [14, 23-24, 37, 48, 53-55]

The principles of treatment for impingement syndrome are initially based on the specificity of the diagnosis in understanding which structure is involved, and also secondary influences contributing to the impingement process. The early stages of care with an acute presentation involve the reduction of the inflammatory process by using modalities such as ice, ultrasound, or interferential stimulation. Oral nonsteroidal antiinflammatory drugs can be of benefit in reducing inflammation and for pain control. At this stage of care, the patient should be instructed to rest from normal or work-sports-related activities, but not function. All activities should be performed below shoulder level and in front of the shoulder. Home instructions should also incorporate the use ice on the area 2 to 3 times per day in the first 24 to 48 hours, with 3 applications of 15 minutes with two 15 minute breaks. In our practice, soft tissue techniques such as ischemic compression and transverse friction are also used to decrease pain and to control specific muscle spasm. Take-home advice, especially after friction, is to ice the area at the above-mentioned frequency.

Once the inflammation and pain start to decrease, gentle stretching can be incorporated. With the elimination of the painful arc and subacromial tenderness, the patient progresses to the strengthening phase to re-establish the force couple mechanism of the scapular and glenohumeral joint. The exercises are initially high repetition in the pain-free range of motion, isometric with an eventual progression to isotonic. The authors commonly use a multicolored Theraband with varied resistances. Sport-specific exercises can be incorporated into the final stages of the program.

Of the electro modalities, the apparatus used was ultrasound, which has been used frequently across the professions in the management of shoulder disorders. Ultrasound has been routinely used by many authors in conjunction with other modalities with positive outcomes. [10, 50, 55] The physiologic effects of ultrasound have been attributed to its thermal actions, which involve increased peripheral blood flow, increased tissue metabolism, and greater tissue extensibility. [56] Evidence exists about the positive and negative aspects of ultrasound therapy, with only a small amount of research investigating its effect on shoulder pain and disorders.

Nykanen [54] investigated pulsed-ultrasound treatment of the painful shoulder in a randomized, double-blind, and placebo-controlled study. The results showed no differences between the treatment and placebo group, but when the ultrasound was used to complement treatment, the patients reported a significant subjective improvement in symptoms. Downing [55] treated supraspinatus tendonitis with a 1-MHz ultrasound unit. The subjects were randomized to receive true or sham ultrasound with the outcome measures being pain, range of motion, and function. The study showed no difference between the ultrasound group and the sham group. Based on these and other studies, one may conclude that ultrasound has little or no apparent benefit in the treatment of shoulder pain. In contrast to the above studies, the subject in this article was treated with a 3-MHz setting plus phonophoresis, which may have influenced the outcome measures.

In this study, the subject was treated with phonophoresis. Phonophoresis involves the movement of a medication through intact skin into the underlying soft tissue by ultrasonic pertubation. [56] The medication used to treat the subjects was a topical corticosteroid-Sigmacort 1% (Sigma Pharmaceuticals Pty Ltd, Clayton, Victoria, Australia). This approach, combined with the therapeutic effects of ultrasound, appeared subjectively to have a beneficial effect as a treatment adjunct. There is some evidence about the positive effects of phonophoresis. Griffin et al [57] conducted a double blind study comparing the effects of phonophoresis and ultrasound in 102 patients with various shoulder complaints. Of the subjects receiving phonophoresis, 68% showed significant improvement in range of motion and pain as opposed to 28% in the ultrasound group. By using ultrasound, a topical corticosteroid cream can be successfully delivered across the skin to reduce the inflammation and pain associated with soft tissue injuries and disorders [58] that are located close to the surface. In the chiropractic literature, 1 article was recently published investigating the benefits of phonophoresis. Gimblet et al [50] reports treating 2 subjects with calcific tendinitis by using soft tissue therapy, phonophoresis, and manipulation. Both subjects at the end of the treatment protocol experienced complete resolution of symptoms.

Steroids are commonly and routinely used in the medical profession for the treatment of shoulder pain, normally in the early stages for pain relief and to combat the inflammatory process. However, such methods generally are not considered to resolve the pathophysiologic features of the condition without proper adjunctive treatment and rehabilitation. [59]

The soft tissue techniques used included ischemic compression and transverse friction massage. Transverse friction massage has been advocated by a number of authors in the management of shoulder disorders. [48, 53, 60] Hammer describes friction massage as a technique in which an involved muscle, tendon or ligament is massaged by applying pressure with a reinforced finger. [48, 53] The transverse motion across the involved tissue and the resultant hyperemia are said to be the chief healing factors of friction massage. [48, 53] The transverse action prevents the formation of scar tissue whereas longitudinal friction effects the transportation of blood and lymph. [48] The traumatic hyperemia results in the release of histamine and bradykinins, resulting in vasodilation and reduction of oedema. [53] Friction massage stimulates the proliferation of fibroblasts and collagen-fiber realignment with cross linkages. [53]

In the acute stage, a gentle friction is applied whilst in more chronic conditions a stronger pressure is required. [48, 53] After treatment, the patients may experience soreness and sensitivity; hence, it is often wise to advise the use of ice over the area of friction application.

The patient in this case report was treated with friction massage across the rotator cuff insertion on the greater tuberosity of the humerus. The patient was positioned supine with the elbow flexed and a small amount of glenohumeral external rotation allowing palpatory exposure of the anterior cuff insertion. Friction was also used across the coracoacromial ligament inferior to the acromioclavicular joint.

A successful management plan must also include orthopedic evaluation, motion assessment and treatment of spinal structures, including the cervical and thoracic spine. In this particular case, a secondary contribution of spinal structures was also noted. The patient had rounded shoulders and anterior head carriage. This pathomechanical process can effect the resting position of the scapula and therefore can create shoulder girdle muscle imbalance, altered muscle length–tension relationships, joint incongruity, ligamentous laxity, arthrokinematics, and changes in gross shoulder motion. [29] According to Greenfield et al, [29] the resultant effect of this type of postural condition is a compensatory extension at the atlantooccipital articulation, reversal or flattening of the cervical lordosis, and an increased midthoracic kyphosis.

Such spinal changes lead to protraction of the scapulae with the inferior angle of the scapula moving medially while the glenoid fossa moves anteriorly and inferiorly, and, finally, the internal rotation of the humerus. The net effects are muscle imbalances of the shoulder girdle. These include parascapular muscle weakness, winging of the scapula, altered scapula position, and scapula dysrhythmia. [28-29] These changes will effect the normal length-tension relationship of the shoulder muscles and will contribute to the generation of posterior cuff muscle weakness that affects the glenohumeral force-couple mechanism. Instead of a balanced couple function, the dominant force vector will be derived from the deltoid muscle, causing superior migration of the humeral head during arm elevation. Normally this process is countered by the action of the cuff muscles, creating a compressive and stabilizing action. Therefore, with cuff weakness, the force couple will be altered, enabling an abnormal upward displacement of the humeral head. This results in the impingement of the subacromial structures and the humeral head against the under surface of the acromion causing irritation of pain-producing structures creating shoulder pain syndromes. To address the abnormal force couple and its causative mechanism, exercises were introduced to restore strength and muscular functioning of glenohumeral joint and scapula articulations once motion was normalized. These exercises initially included isometric strengthening of the rotator cuff muscles, with progression to isotonic rotator cuff and parascapular muscle exercises.

Conclusion

This article highlights a successful outcome for a patient with shoulder impingement syndrome after receiving a multimodal treatment approach combining soft tissue techniques (ischemic compression, friction), electromodalites (ultrasound), manipulation, and rehabilitation (exercises). In managing the shoulder and shoulder pain syndromes, a detailed knowledge of the anatomy of the shoulder and associated structures including the scapulohumeral, scapulothoracic articulations, the cervical, and the thoracic spine is important to develop an appropriate treatment plan. The practitioner is therefore well placed to manage both shoulder and spinal pain syndromes. Recent evidence suggests that this may be the future direction in managing pain of musculoskeletal origin, [53] particularly of the shoulder. [48] To determine the true effectiveness of a multimodal chiropractic treatment approach, further research should be initiated.